KLF6 contributes to myeloid cell plasticity in the pathogenesis of intestinal inflammation.

ABSTRACT: Inflammatory bowel disease (IBD) is associated with dysregulated macrophage responses, such that quiescent macrophages acquire a pro-inflammatory activation state and contribute to chronic intestinal inflammation. The transcriptional events governing macrophage activation and gene expression in the context of chronic inflammation such as IBD remain incompletely understood. Here, we identify Kruppel-like transcription factor-6 (KLF6) as a critical regulator of pathogenic myeloid cell activation in human and experimental IBD. We found that KLF6 was significantly upregulated in myeloid cells and intestinal tissue from IBD patients and experimental models of IBD, particularly in actively inflamed regions of the colon. Using complementary gain- and loss-of-function studies, we observed that KLF

SUBMITTER: Goodman WA 

PROVIDER: S-EPMC4972715 | biostudies-literature | 2016 Sep

REPOSITORIES: biostudies-literature